Chapter 13. Memory, Learning, and Development

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National Institutes of Health scientists have used human skin cells to create what they believe is the first cerebral organoid system, or “mini-brain,” for studying sporadic Creutzfeldt-Jakob disease (CJD). CJD is a fatal neurodegenerative brain disease of humans believed to be caused by infectious prion protein. It affects about 1 in 1 million people. The researchers, from NIH’s National Institute of Allergy and Infectious Diseases (NIAID), hope the human organoid model will enable them to evaluate potential therapeutics for CJD and provide greater detail about human prion disease subtypes than the rodent and nonhuman primate models currently in use. Human cerebral organoids are small balls of human brain cells ranging in size from a poppy seed to a small pea. Their organization, structure, and electrical signaling are similar to brain tissue. Because these cerebral organoids can survive in a controlled environment for months, nervous system diseases can be studied over time. Cerebral organoids have been used as models to study Zika virus infection, Alzheimer’s disease, and Down syndrome. In a new study published in Acta Neuropathologica Communications, scientists at NIAID’s Rocky Mountain Laboratories discovered how to infect five-month-old cerebral organoids with prions using samples from two patients who died of two different CJD subtypes, MV1 and MV2. Infection took about one month to confirm, and the scientists monitored the organoids for changes in health indicators, such as metabolism, for more than six months. By the end of the study, the scientists observed that seeding activity, an indication of infectious prion propagation, was present in all organoids exposed to the CJD samples. However, seeding was greater in organoids infected with the MV2 sample than the MV1 sample. They also reported that the MV1-infected organoids showed more damage than the MV2-infected organoids.

Keyword: Prions; Development of the Brain
Link ID: 26331 - Posted: 06.15.2019

By Simon Makin Better Memory through Electrical Brain Ripples Hippocampus Neuron, computer illustration Credit: Kateryna Kon Getty Images Specific patterns of brain activity are thought to underlie specific processes or computations important for various mental faculties, such as memory. One such “brain signal” that has received a lot of attention recently is known as a “sharp wave ripple”—a short, wave-shaped burst of high-frequency oscillations. Researchers originally identified ripples in the hippocampus, a region crucially involved in memory and navigation, as central to diverting recollections to long-term memory during sleep. Then a 2012 study by neuroscientists at the University of California, San Francisco, led by Loren Frank and Shantanu Jadhav, the latter now at Brandeis University, showed that the ripples also play a role in memory while awake. The researchers used electrical pulses to disrupt ripples in rodents’ brains, and showed that, by doing so, performance in a memory task was reduced. However, nobody had manipulated ripples to enhance memory—until now, that is. Researchers at NYU School of Medicine led by neuroscientist György Buzsáki have now done exactly that. In a June 14 study in Science, the team showed that prolonging sharp wave ripples in the hippocampus of rats significantly improved their performance in a maze task that taxes working memory—the brain’s “scratch pad” for combining and manipulating information on the fly. “This is a very novel and impactful study,” says Jadhav, who was not involved in the research. “It’s very hard to do ‘gain-of-function’ studies with physiological processes in such a precise way.” As well as revealing new details about how ripples contribute to specific memory processes, the work could ultimately have implications for efforts to develop interventions for disorders of memory and learning. © 2019 Scientific American

Keyword: Learning & Memory
Link ID: 26330 - Posted: 06.15.2019

By Caterina Gawrilow, Sara Goudarzi Those affected by attention deficit hyperactivity disorder (ADHD) are clinically thought of as inattentive, hyperactive and impulsive. However, people with ADHD are also perceived as being very spontaneous, curious, inquisitive, enthusiastic, lively and witty, a perception that creates an impression they are more creative than those without ADHD. But is there truth to this idea? Creativity is generally the ability to generate something original and unprecedented. The ideas must not only be new and surprising, but also useful and relevant. Among other things, creativity comes through intensive knowledge and great motivation in a particular field, be it painting, music or mathematics. For years, both laypersons and scientists have been fascinated by the proverbial proximity of genius and madness. According to psychologist Dean Keith Simonton from the University of California, Davis, unusual and unexpected experiences, such as psychological difficulties and psychiatric stays, are an important characteristic of people who create masterpieces. Advertisement Two core symptoms, inattention and impulsiveness, suggest a connection between creativity and ADHD. Inattention, which occurs more frequently in those affected with the disorder, likely leads to mind wandering, or the drifting of thoughts from an activity or environment. Such drifting can lead to new, useful and creative ideas. © 2019 Scientific American

Keyword: ADHD
Link ID: 26324 - Posted: 06.12.2019

Katarina Zimmer Occasionally, as the nematode worm C. elegans meanders across rotten fruit on the prowl for bacteria to eat, it comes across ones it shouldn’t dine on. Some bacteria are lethal to the animals when ingested, and unfortunately, the worms can’t always distinguish them from the nutritious kind until it’s too late. Nevertheless, this doesn’t stop them from teaching their young not to make the same mistake, researchers recently realized when watching the nematodes in the lab. Before the animals die from the pathogen, they often lay eggs. These offspring, researchers at Princeton University observed, consistently avoid that particular bacterial species. Evidently, pathogen avoidance—a behavioral habit the mothers learned towards the end of their lifetime—can be transmitted to the next generation, aiding their survival. But it’s not a hard-wired trait; instead, an epigenetic mechanism involving small RNAs appears to be responsible. That’s the finding of a paper published in Cell yesterday (June 6). Alongside it in the journal, a group at Tel Aviv University also reports on transgenerational inheritance of behavior traits in C. elegans. This team took a different approach, demonstrating how a small RNA–based mechanism allows information from the nervous system to be transmitted to germline cells and into future generations. While it’s known that traits involved in immunity and stress can be inherited across generations in C. elegans, the two papers are among the first to show that complex behaviors can be transmitted in the same way. © 1986–2019 The Scientist

Keyword: Epigenetics
Link ID: 26322 - Posted: 06.11.2019

By Jane E. Brody How did you sleep last night? If you’re over 65, I hope it was better than many others your age. In a study by the National Institute on Aging of over 9,000 Americans aged 65 and older, more than half said they had difficulty falling asleep or staying asleep. Many others who believe they spend an adequate number of hours asleep nonetheless complain of not feeling rested when they get up. Chronic insomnia, which affects 5 percent to 10 percent of older adults, is more than just exhausting. It’s also linked to an increased risk of developing hypertension, Type 2 diabetes, heart attack, depression, anxiety and premature death. It may also be a risk factor for dementia, especially Alzheimer’s disease. Studies based on more than 1,700 men and women followed over many years by researchers at Pennsylvania State University College of Medicine found that the risk of developing hypertension was five times greater among those who slept less than five hours a night and three and a half times greater for those who slept between five and six hours. But there was no increased risk among those who regularly slept six or more hours. Likewise, the risk of developing diabetes was three times greater for the shortest sleepers and twice as great for those who slept between five and six hours. People with insomnia often complain that they can’t concentrate or focus and have memory problems. While the evidence for this is inconsistent, the Penn State studies showed that people with insomnia are more likely to perform poorly on tests of processing speed, switching attention and visual memory. And most studies have shown that insomnia impairs cognitive performance, a possible risk factor for mild cognitive impairment and dementia. © 2019 The New York Times Company

Keyword: Sleep; Alzheimers
Link ID: 26315 - Posted: 06.10.2019

By Aiyana Bailin To my dismay, Simon Baron-Cohen’s recent article “The Concept of Neurodiversity is Dividing the Autism Community” perpetuates a common misunderstanding of the neurodiversity movement: that it views autism as a difference but not a disability. Baron-Cohen presents the issue as one of opposing sides: the medical model, which sees autism as a set of symptoms and deficits to be cured or treated, and the neurodiversity model, which he believes ignores any disabling aspects of autism. Unfortunately, this confuses the neurodiversity movement with the social model of disability, and it is an incomplete understanding of the social model at that. Before I go into details, let me summarize what the neurodiversity movement does believe: Autism and other neurological variations (learning disabilities, ADHD, etc.) may be disabilities, but they are not flaws. People with neurological differences are not broken or incomplete versions of normal people. Disability, no matter how profound, does not diminish personhood. People with atypical brains are fully human, with inalienable human rights, just like everyone else. People with disabilities can live rich, meaningful lives. Neurological variations are a vital part of humanity, as much as variations in size, shape, skin color and personality. None of us has the right (or the wisdom) to try and improve upon our species by deciding which characteristics to keep and which to discard. Every person is valuable. Disability is a complicated thing. Often, it’s defined more by society’s expectations than by individual conditions. Not always, but often. © 2019 Scientific American

Keyword: Autism
Link ID: 26310 - Posted: 06.07.2019

By Christopher Rowland A team of researchers inside Pfizer made a startling find in 2015: The company’s blockbuster rheumatoid arthritis therapy Enbrel, a powerful anti-inflammatory drug, appeared to reduce the risk of Alzheimer’s disease by 64 percent. The results were from an analysis of hundreds of thousands of insurance claims. Verifying that the drug would actually have that effect in people would require a costly clinical trial — and after several years of internal discussion, Pfizer opted against further investigation and chose not to make the data public, the company confirmed. Researchers in the company’s division of inflammation and immunology urged Pfizer to conduct a clinical trial on thousands of patients, which they estimated would cost $80 million, to see if the signal contained in the data was real, according to an internal company document obtained by The Washington Post. “Enbrel could potentially safely prevent, treat and slow progression of Alzheimer’s disease,’’ said the document, a PowerPoint slide show that was prepared for review by an internal Pfizer committee in February 2018. The company told The Post that it decided during its three years of internal reviews that Enbrel did not show promise for Alzheimer’s prevention because the drug does not directly reach brain tissue. It deemed the likelihood of a successful clinical trial to be low. A synopsis of its statistical findings prepared for outside publication, it says, did not meet its “rigorous scientific standards.’’ The surprising reasons why drug prices in the U.S. are higher than in the rest of the world © 1996-2019 The Washington Post

Keyword: Alzheimers
Link ID: 26307 - Posted: 06.06.2019

Children can keep full visual perception — the ability to process and understand visual information — after brain surgery for severe epilepsy, according to a study funded by the National Eye Institute (NEI), part of the National Institutes of Health. While brain surgery can halt seizures, it carries significant risks, including an impairment in visual perception. However, a new report by Carnegie Mellon University, Pittsburgh, researchers from a study of children who had undergone epilepsy surgery suggests that the lasting effects on visual perception can be minimal, even among children who lost tissue in the brain’s visual centers. Normal visual function requires not just information sent from the eye (sight), but also processing in the brain that allows us to understand and act on that information (perception). Signals from the eye are first processed in the early visual cortex, a region at the back of the brain that is necessary for sight. They then travel through other parts of the cerebral cortex, enabling recognition of patterns, faces, objects, scenes, and written words. In adults, even if their sight is still present, injury or removal of even a small area of the brain’s vision processing centers can lead to dramatic, permanent loss of perception, making them unable to recognize faces, locations, or to read, for example. But in children, who are still developing, this part of the brain appears able to rewire itself, a process known as plasticity. “Although there are studies of the memory and language function of children who have parts of the brain removed surgically for the treatment of epilepsy, there have been rather few studies that examine the impact of the surgery on the visual system of the brain and the resulting perceptual behavior,” said Marlene Behrmann, Ph.D., senior author of the study. “We aimed to close this gap.”

Keyword: Development of the Brain; Vision
Link ID: 26303 - Posted: 06.05.2019

Nell Greenfieldboyce At the Marine Biological Laboratory in Woods Hole, Mass., there's a room filled with burbling aquariums. A lot of them have lids weighed down with big rocks. "Octopuses are notorious for being able to, kind of, escape out of their enclosures," says Bret Grasse, whose official title at MBL is "manager of cephalopod operations" — cephalopods being squid, cuttlefish and octopuses. He's part of a team that's trying to figure out the best ways to raise these sea creatures in captivity, so that scientists can investigate their genes and learn the secrets of their strange, almost alien ways. For decades, much of the basic research in biology has focused on just a few, well-studied model organisms like mice, fruit flies, worms and zebrafish. That's because these critters are easy to keep in the laboratory, and scientists have worked out how to routinely alter their genes, leading to all kinds of insights into behavior, diseases and possible treatments. "With these organisms, you could understand what genes did by manipulating them," says Josh Rosenthal, another biologist at MBL. "And that really became an indispensable part of biology." But it's also meant that basic biology has ignored much of the animal kingdom, especially its more exotic denizens. "We're really missing out on, I would say, the diversity of biology's solutions to problems," Rosenthal notes. © 2019 npr

Keyword: Learning & Memory; Evolution
Link ID: 26295 - Posted: 06.04.2019

by Jessica Wright Spontaneous mutations that occur between genes are as important in autism as those within genes, a new study suggests1. The study, published today in Nature Genetics, is the first to look at the impact of these ‘noncoding’ mutations across the whole genomes of autistic people. Many teams over the past three years have sequenced the DNA of autistic people both within and between genes. Yet sorting through the hundreds of thousands of mutations between genes had seemed nearly impossible because researchers know so little about these genetic segments. The new study overcomes this challenge by using a machine-learning approach. The researchers created an algorithm that predicts whether a particular noncoding mutation alters any gene’s expression. It assigns each mutation a score based on how likely it is to do so — and to be harmful. “The unique approach here is that instead of just counting mutations, we’re using the deep-learning-based frameworks to look at their regulatory impacts,” says co-lead author Olga Troyanskaya, professor of integrative genomics at Princeton University in New Jersey. “All mutations are not created equal, and all effects are not created equal.” (Troyanskaya also holds a position at the Simons Foundation, Spectrum’s parent organization.) A strength of the study is that it looks at spontaneous mutations across the entire genome, experts say. © 2019 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 26291 - Posted: 06.03.2019

Kerry Grens In mice whose sense of smell has been disabled, a squirt of stem cells into the nose can restore olfaction, researchers report today (May 30) in Stem Cell Reports. The introduced “globose basal cells,” which are precursors to smell-sensing neurons, engrafted in the nose, matured into nerve cells, and sent axons to the mice’s olfactory bulbs in the brain. “We were a bit surprised to find that cells could engraft fairly robustly with a simple nose drop delivery,” senior author Bradley Goldstein of the University of Miami Miller School of Medicine says in a press release. “To be potentially useful in humans, the main hurdle would be to identify a source of cells capable of engrafting, differentiating into olfactory neurons, and properly connecting to the olfactory bulbs of the brain. Further, one would need to define what clinical situations might be appropriate, rather than the animal model of acute olfactory injury.” Goldstein and others have independently tried stem cell therapies to restore olfaction in animals previously, but he and his coauthors note in their study that it’s been difficult to determine whether the regained function came from the transplant or from endogenous repair stimulated by the experimental injury to induce a loss of olfaction. So his team developed a mouse whose resident globose basal cells only made nonfunctional neurons, and any restoration of smell would be attributed to the introduced cells. © 1986–2019 The Scientist

Keyword: Chemical Senses (Smell & Taste); Stem Cells
Link ID: 26285 - Posted: 06.01.2019

By Kelly Servick Genes are a powerful driver of risk for autism, but some researchers suspect another factor is also at play: the set of bacteria that inhabits the gut. That idea has been controversial, but a new study offers support for this gut-brain link. It reveals that mice develop autismlike behaviors when they are colonized by microbes from the feces of people with autism. The result doesn’t prove that gut bacteria can cause autism. But it suggests that, at least in mice, the makeup of the gut can contribute to some hallmark features of the disorder. “It’s quite an encouraging paper,” says John Cryan, a neuroscientist at University College Cork in Ireland who was not involved in the research. The idea that metabolites—the molecules produced by bacterial digestion—can influence brain activity “is plausible, it makes sense, and it will help push the field forward.” Many studies have found differences between the composition of the gut microbiomes in people with and without autism. But those studies can’t determine whether a microbial imbalance is responsible for autism symptoms or is a result of having the condition. To test the effect of the gut microbiome on behavior, Sarkis Mazmanian, a microbiologist at the California Institute of Technology (Caltech) in Pasadena, and collaborators put fecal samples from children with and without autism into the stomachs of germ-free mice, which had no microbiomes of their own. The researchers then mated pairs of mice colonized with the same microbiomes, so their offspring would be exposed to a set of human microbes early in development. © 2019 American Association for the Advancement of Science

Keyword: Autism
Link ID: 26283 - Posted: 05.31.2019

By George Musser, Even the slightest touch can consume Kirsten Lindsmith’s attention. When someone shakes her hand or her cat snuggles up against her, for example, it becomes hard for her to think about anything else. “I’m taken out of the moment for however long the sensation lasts,” she says. Some everyday sensations, such as getting her hands wet, can feel like torture: “I usually compare it to the visceral, repulsive feeling you’d get plunging your hand into a pile of rotting garbage,” says the 27-year-old autistic writer. Stephanie Dehennin, an autistic illustrator who lives in Belgium, detests gentle touches but doesn’t mind firm hugs. “I will feel actual rage if someone strokes me or touches me very lightly,” she says. Dehennin seeks out deep pressure to relieve her stress. “I’ll sit between my bed and my nightstand, for example — squeezed between furniture.” Strong reactions to touch are remarkably widespread among people who have autism, despite the condition’s famed heterogeneity. “The touch thing is as close to universal as they come,” says Gavin Bollard, an autistic blogger who lives in Australia and writes about his and his autistic sons’ experiences. These responses are often described as a general hypersensitivity, but they are more complex than that: Sometimes autistic people crave touch; sometimes they cringe from it. For many people on the spectrum, these sensations are so intense that they take measures to shape their ‘touchscape.’ Some pile on heavy blankets at night for the extra weight; others cut off their clothing tags. © 2019 American Association for the Advancement of Science

Keyword: Autism; Emotions
Link ID: 26281 - Posted: 05.30.2019

/ By Jennie Erin Smith Piedad’s house sits above the cemetery in Girardota, Colombia, just north of Medellín. From her front porch, the view gives way to green hills, each home to hamlets with sugarcane plots and tile-roofed houses tucked in among the trees. One of these hillside hamlets is where Piedad and her 11 siblings grew up. Their father, Horacio, worked in cane fields and sugar mills, and their mother sold fruit from her orchard; their grandmother made pots from clay she dug across the river. When earthquakes destroyed their home in 1979, the family moved into town and left rural life behind. Why should two families with parallel mutations co-exist in one tiny corner of the Andes? Horacio showed the first symptoms of dementia soon afterward. He ignored the food he was served and got lost returning from church. He grew aggressive and delusional, and Piedad would return from her job at a sugar-packing plant to help bathe him, holding back tears as he kicked and punched. Horacio died in 1984 from what his doctors called senile dementia, the same disease that killed his father and three of his siblings. By the early 2000s, four of Piedad’s own siblings, then in their 40s and 50s, were showing signs of dementia. A local doctor referred them to a group of investigators in Medellín who studied families with a unique genetic mutation that causes early-onset Alzheimer’s disease. Nicknamed the Paisa mutation after the people of Colombia’s Antioquia region, who call themselves paisas, it occurred on a gene, called presenilin-1, implicated in familial Alzheimer’s. The families affected tended to be white farmers living in remote mountain towns that felt untouched by time. Copyright 2019 Undark

Keyword: Alzheimers; Genes & Behavior
Link ID: 26271 - Posted: 05.28.2019

Laura Sanders A teenager’s brain does not magically mature into its reasoned, adult form the night before his or her 18th birthday. Instead, aspects of brain development stretch into a person’s 20s — a protracted fine-tuning with serious implications for young people caught in the U.S. justice system, argues cognitive neuroscientist B.J. Casey of Yale University. In the May 22 Neuron, Casey describes the heartbreaking case of Kalief Browder, sent at age 16 to Rikers Island correctional facility in New York City after being accused of stealing a backpack. Unable to come up with the $3,000 bail, Browder spent three years in the violent jail before his case was ultimately dropped. About two-thirds of his time in custody was spent in solitary confinement — “a terrible place for a child to have to grow up,” Casey says. Two years after his 2013 release, Browder died from suicide. Casey uses the case to highlight how the criminal justice system — and the accompanying violence, stress and isolation (SN: 12/8/18, p. 11) that come with being incarcerated — can interfere with brain development in adolescents and children. Other recent stories of immigrant children being separated from their families and held in detention centers have raised similar concerns (SN Online: 6/20/18). Studies with lab animals and brain imaging experiments in people show that chronic stress and other assaults “impact the very brain circuitry that is changing so radically during adolescence,” Casey says. An abundance of science says that “the way we’re treating our young people is not the way to a healthy development.” |© Society for Science & the Public 2000 - 2019

Keyword: Development of the Brain; Stress
Link ID: 26262 - Posted: 05.23.2019

Ed Yong In 1996, a group of European researchers found that a certain gene, called SLC6A4, might influence a person’s risk of depression. It was a blockbuster discovery at the time. The team found that a less active version of the gene was more common among 454 people who had mood disorders than in 570 who did not. In theory, anyone who had this particular gene variant could be at higher risk for depression, and that finding, they said, might help in diagnosing such disorders, assessing suicidal behavior, or even predicting a person’s response to antidepressants. Back then, tools for sequencing DNA weren’t as cheap or powerful as they are today. When researchers wanted to work out which genes might affect a disease or trait, they made educated guesses, and picked likely “candidate genes.” For depression, SLC6A4 seemed like a great candidate: It’s responsible for getting a chemical called serotonin into brain cells, and serotonin had already been linked to mood and depression. Over two decades, this one gene inspired at least 450 research papers. But a new study—the biggest and most comprehensive of its kind yet—shows that this seemingly sturdy mountain of research is actually a house of cards, built on nonexistent foundations. Richard Border of the University of Colorado at Boulder and his colleagues picked the 18 candidate genes that have been most commonly linked to depression—SLC6A4 chief among them. Using data from large groups of volunteers, ranging from 62,000 to 443,000 people, the team checked whether any versions of these genes were more common among people with depression. “We didn’t find a smidge of evidence,” says Matthew Keller, who led the project. (c) 2019 by The Atlantic Monthly Group.

Keyword: Depression; Genes & Behavior
Link ID: 26261 - Posted: 05.22.2019

By Kenneth Miller A model of Ben Barres’ brain sits on the windowsill behind his desk at Stanford University School of Medicine. To a casual observer, there’s nothing remarkable about the plastic lump, 3-D-printed from an MRI scan. Almost lost in the jumble of papers, coffee mugs, plaques and trophies that fill the neurobiologist’s office, it offers no hint about what Barres’ actual gray matter has helped to accomplish: a transformation of our understanding of brains in general, and how they can go wrong. Barres is a pioneer in the study of glia. This class of cells makes up 90 percent of the human brain, but gets far less attention than neurons, the nerve cells that transmit our thoughts and sensations at lightning speed. Glia were long regarded mainly as a maintenance crew, performing such unglamorous tasks as ferrying nutrients and mopping up waste, and occasionally mounting a defense when the brain faced injury or infection. Over the past two decades, however, Barres’ research has revealed that they actually play central roles in sculpting the developing brain, and in guiding neurons’ behavior at every stage of life. “He has made one shocking, revolutionary discovery after another,” says biologist Martin Raff, emeritus professor at University College London, whose own work helped pave the way for those advances. Recently, Barres and his collaborators have made some discoveries that may revolutionize the treatment of neurodegenerative ailments, from glaucoma and multiple sclerosis to Alzheimer’s disease and stroke. What drives such disorders, their findings suggest, is a process in which glia turn from nurturing neurons to destroying them. Human trials of a drug designed to block that change are just beginning.

Keyword: Glia; Learning & Memory
Link ID: 26258 - Posted: 05.22.2019

by C.L. Lynch Everyone knows that autism is a spectrum. People bring it up all the time. “My son is on the severe end of the autism spectrum.” “We’re all a little autistic– it’s a spectrum.” “I’m not autistic but I’m definitely ‘on the spectrum.'” If only people knew what a spectrum is… because they are talking about autism all wrong. Let’s use the visible spectrum as an example. As you can see, the various parts of the spectrum are noticeably different from each other. Blue looks very different from red, but they are both on the visible light spectrum. Red is not “more blue” than blue is. Red is not “more spectrum” than blue is. When people discuss colours, they don’t talk about how “far along” the spectrum a colour is. They don’t say “my walls are on the high end of the spectrum” or “I look best in colours that are on the low end of the spectrum.” But when people talk about autism they talk as if it were a gradient, not a spectrum at all. People think you can be “a little autistic” or “extremely autistic,” the way a paint colour could be a little red or extremely red. An image of a colour gradient moving from white to red. The lightest zone is labelled How people think the spectrum looks But autism isn’t that simple. Autism isn’t a set of defined symptoms that collectively worsen as you move “up” the spectrum.

Keyword: Autism
Link ID: 26254 - Posted: 05.21.2019

By Nathaniel Scharping | Don’t get a big head, your mother may have told you. That’s good advice, but it comes too late for most of us. Humans have had big heads, relatively speaking, for hundreds of thousands of years, much to our mothers’ dismay. Our oversize noggins are a literal pain during childbirth. Babies have to twist and turn as they exit the birth canal, sometimes leading to complications that necessitate surgery. And while big heads can be painful for the mother, they can downright transformative for babies: A fetus’ pliable skull deforms during birth like putty squeezed through a tube to allow it to pass into the world. This cranial deformation has been known about for a long time, but in a new study, scientists from France and the U.S. actually watched it happen using an MRI machine during labor. The images, published in a study in PLOS One, show how the skulls (and brains) of seven infants squished and warped during birth to pass through the birth canal. They also shine new light on how much our skulls change shape as we’re born. The researchers recruited pregnant women in France to undergo an MRI a few weeks before pregnancy and another in the minutes before they began to actually give birth. In total, seven women were scanned in the second stage of labor, when the baby begins to make its way out of the uterus. They were then rushed to the maternity ward to actually complete giving birth.

Keyword: Development of the Brain; Brain imaging
Link ID: 26252 - Posted: 05.20.2019

Before he was born, his parents knew their boy was in trouble. That was clear from what their doctors' saw in their baby's ultrasound. And tragically, the boy died when he was only ten months old. But in his short life, he left behind a valuable legacy by helping scientists understand a crucial type of brain cell. That's because — as it turned out — the child had none. "One of the things about being a pediatric geneticist is on any given day you can see a patient you could spend the rest of your life or your career thinking about," Dr. James Bennett told Quirks & Quarks host Bob McDonald. Dr. Bennett is a physician and researcher from Seattle Children's Hospital and assistant professor of pediatric genetics at the University of Washington. Devastating problems with brain development On the first day he met the child — the boy's very first day of life — Dr. Bennett said he could tell this baby needed a lot of support. The baby was having difficulty breathing, had an enlarged head as well as some very significant abnormalities of his brain. "Every single part of his brain was affected. There was no connection between the left side and the right side of his brain. And there was too much fluid on the brain — that the spaces that hold fluid around the brain were enlarged. And the white matter, which is the part of the brain that sort of connects the neurons — you can think of it as sort of the wires connecting things in the brain — was decreased and abnormal," said Dr. Bennett. Scientists had never seen a medical mystery like this before, so Dr. Bennett was determined to figure out what was wrong with the infant. He he undertook a "diagnostic odyssey" to identify the cause of this extremely rare condition. ©2019 CBC/Radio-Canada

Keyword: Development of the Brain; Glia
Link ID: 26251 - Posted: 05.20.2019